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Figure 1. Mechanistic overview of ncRNAs in cardiovascular aging and disease. (A) Summarizes how miRNAs, lncRNAs, circRNAs, piRNAs, and tsRNAs converge on endothelial dysfunction, vascular smooth muscle phenotypic switching, inflammation and immune aging, fibrosis and extracellular matrix remodeling, and oxidative stress or mitochondrial dysfunction; (B) Highlights representative ncRNA mechanisms, including miR-21-SPRY1/TGFβ-driven fibrotic remodeling, miR-126-VEGF/PI3K-AKT-mediated angiogenesis and repair, MHRT-mediated BRG1 repression, circANRIL-associated rRNA maturation, and piRNA/tsRNA-mediated epigenetic and mitochondrial control. lncRNAs: Long noncoding RNAs; circRNAs: circular RNAs; piRNAs: piwi-interacting RNAs; tsRNAs: transfer RNA-derived small RNAs; rRNA: ribosomal RNA; miRNAs: microRNAs; ECM: extracellular matrix; VSMC: vascular smooth muscle cell; MHRT: myosin heavy chain associated RNA transcript; BRG1: brahma-related gene 1; VEGF: vascular endothelial growth factor; circANRIL: circular antisense non-coding RNA in the INK4 locus; SPRY1: sprouty RTK signaling antagonist; TGFβ: transforming growth factor-beta; PI3K: phosphoinositide 3-kinase; AKT: protein kinase B.